Renal complications are often detected in patients with inflammatory bowel disease (IBD). Because conventional markers such as serum creatinine and β2-microglobulin are not sensitive and/or specific, a new renal biomarker is needed. We have recently identified urinary vanin-1 as an early biomarker for the detection of nephrotoxicant-induced renal injury. In this study, we compared the usefulness of urinary vanin-1 with other newly developed biomarkers [urinary monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (Kim-1) and N-acetyl-beta-D-glucosaminidase (NAG)] for the detection of renal complications in rats with experimental colitis. On day 2 after intracolonic injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS), male Wistar rats developed not only colitis, but histologically evident renal injury. Urinary vanin-1 started to elevate on day 1, whereas serum creatinine and urinary excretions of glucose, total protein, albumin, Kim-1, MCP-1 and NAG significantly increased only on day 2. The mRNA expressions of vanin-1 and Kim-1 significantly increased in the kidney, but not in the colon. In addition, vanin-1 did not appear in the blood. On the other hand, colonic mRNA expression and the serum concentration of MCP-1 were significantly higher in the TNBS-treated rats than in the control animals. These results suggest that, in contrast to MCP-1, urinary vanin-1 and Kim-1 mainly originated from the kidney rather than the colon in this model. Compared with Kim-1 and MCP-1, vanin-1 might be an earlier biomarker for the detection of renal injury in rats with experimental colitis.
No takes yet. Share an insight, caveat, or question.
Hosohata et al. (2013) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: